Work has progressed on the accumulation of pharmacological evidence that synaptic vesicle membranes can fuse or attach to the axolemma to form a new structure containing the amine-transporting mechanisms of both membranes. Rat heart ventricle slices incubated in a choline and Ca++ (Ch+-Ca++) medium secrete norepinephrine (NE) and the secretion is inhibited by cocaine and ATP. The effect of ATP is antagonized by reserpine, which is known to block the Mg++ATP activation of the pump in the vesicle membrane. Lithium, as supplement to Ch+- Ca++, stimulates the release of 3H-amine. The release is inhibited by cocaine. These characteristics of Li+ are opposite to the usual characteristics observed when Li+ is used alone as a Na+ replacement in Na+-deficient media. The effects of Li+ are in accord with the hypothesis that Li+ acts on vesicles to mobilize and release bound NE. In extensions of previously reported investigations, K+ antagonizes the Na+-dependent binding of transport inhibitors by tissues after the effects of Ch+-Ca++ have been produced. Potassium did not evoke this effect during the preincubation period in KRB. Moreover, K+ did not antagonize the uptake inhibiting effects of the inhibitors. Efforts to detect a Na+-dependency for the binding of cocaine to the transport-carrier in the axolemma were unsuccessful. It has also been concluded that the widely used term "Na+- deprivation" is a misnomer. Electrolytes used as Na+-replacements elicit distinct effects on NE retention.